Key result
Kcne2 deletion in mice basolaterally reroutes parietal cell Kcnq1, driven by a ~5-fold Kcne3 increase.
Population
Mice with targeted deletion of Kcne2 (Kcne2-/- or Kcne2+/-) and/or Kcne3 (Kcne2-/-Kcne3-/-)
Comparison
Targeted deletion of Kcne2 and/or Kcne3 genes vs Wild-type mice (implied)
Design
Preclinical
Authors
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Does not support clinical translation of Kcne2 targeting; leaves open whether Kcne3 remodeling alters human parietal cell function.
This preclinical study demonstrates in vivo Kcne-dependent alpha subunit polarized trafficking and the functional consequences of potassium channel beta subunit remodeling in gastric parietal cells.
Roepke et al. (2010) studied Gastric neoplasia and hypochlorhydria (mouse model). Targeted deletion of Kcne2 and/or Kcne3 vs. Wild-type or control mice was evaluated on Kcne3 expression and Kcnq1 localization. Targeted deletion of Kcne2 in mice basolaterally rerouted the Kcnq1 alpha subunit in parietal cells and upregulated Kcne3 (5.3-fold protein increase), which actively drove this rerouting.
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